The free radical theory of aging typifies aging as an outcome of indiscriminate, random, and cumulative damage to different cellular components caused by reactive oxygen species (ROS). Mitochondrial protection from free radical damage as offered by the enzyme Manganese superoxide dismutase (MnSOD) is indispensable, since mitochondria handle the bulk of intracellular oxygen, the long-term goal of this study is to elucidate the role of MnSOD activity in aging and tissue degeneration thereof. The fruitfly Drosophila melanogaster deploys a defense system to fight against ROS that is very similar to that of humans and previous studies of aging in Drosophila have indicated the importance of antioxidant enzymes in maximum life span extension. The foremost objective of this dissertation work was to obtain a complete loss of function mutation for MnSOD gene in Drosophila. As expected, a complete loss of MnSOD function confers severely reduced lifespan leading to neonatal lethality in Drosophila, same in mouse. This MnSOD mutant model will now enable me to (1) investigate the effect of anti-oxidant activity during development because the severity of the homozygote phenotype seen-death within 24 hours clearly suggest residual effect from development; (2) investigate the effect of loss of MnSOD function in specific tissue or cell types, testing the hypothesis that loss of MnSOD function is associated with increased oxidative stress causing accelerated tissue damages. Thus, with the help of some unique moleculargenetic tools available in Drosophila, my Ph.D dissertation work will enable me to answer several previously unanswered questions related to the biology of aging process. [unreadable] [unreadable]